This is an investigation of the autoimmnity in rheumatoid arthritis (RA). One aim is to determine in hemolytic plaque forming cell assays whether anti IgG autoantibodies, rheumatoid factors (RF), arise because of loss of T cell suppressor function, imposition of T cell helper function, or direct B cell stimulation. A second aim will be to assess the possible role of EB virus in provoking RA, assessing this both in vitro by its behavior in RA cells in culture (including RF production), and in vivo by the time relationships between periods of activation of the disease and antibody arises to EB virus antigens or RA-associated nuclear antigens generated in lymphocytes by EB virus. The third aim will be to determine in serial clinical studies whether RF, or other antibodies forming immune complexes, make up the pathogenetically significant immune complexes in RA.